Chronic Wounds

Normal Skin Flora
The skin is covered with microorganisms. These can be either resident organisms, those that can typically be found on the subject’s skin, or transients that are often seen on the skin surface but are quickly shed during normal body hygiene or by skin sloughing. While these organisms are usually bacteria, the yeast Pityrosporum and skin mite Demodex are also commonly found. These colonizing microbes take residence in the crypts and crevices that favor bacterial growth, and prevent pathologic species from gaining access to these areas. Human beings are protected from bacterial overgrowth and invasion at the surface by a number of defense mechanisms. A layer of dead, keratinous epithelial cells known as the stratum corneum is the outermost layer of skin. As the keratin sloughs, it removes attached organisms with it. Sebaceous glands secrete an oily, lipid-rich, acidic substance, (pH range of 4.2 to 5.6) that acts to retard bacterial growth. Bacteria become more active on the skin surface as the pH rises above 6.5, as is seen with the use of many cleansing and moisturizing agents. Should foreign organisms get past these defenses, the antigen-presenting Langerhans cells found in the epidermis and the phagocytosing macrophages and immune-stimulating mast cells present in the dermis rapidly mobilize the body’s cellular and humoral immune responses.

Contamination vs. Infection
Cutaneous wounds, by definition, have lost their protective barrier and are subject to invasion by not only foreign bacteria introduced through the environment,

Bacteria
Staphylococcus Micrococcus Peptococcus Corynebacterium Brevibacterium Propionibacterium Streptococcus Neisseria Acinetobacter but also the local bacterial flora that is present on intact skin.

These wounds occur in the setting of various pathologies and are usually chronic in nature before being brought to the attention of a plastic surgeon. Unlike most surgical incisions, these wounds heal by secondary intention and are always colonized by bacteria. They require extensive granulation tissue formation and keratinocyte migration for closure, involving endothelial cells and fibroblasts for the purposes of neovascularization and matrix production, respectively. For this to occur, macrophages and a varying milieu of growth factors must be present. Along with neutrophils, macrophages also act to disinfect the wound, killing foreign organisms by the generation of peroxide and superoxide radicals. The clinical spectrum of bacterial invasion exists on a continuum from least to most severe: contamination, colonization, local infection or critical contamination, invasive infection and sepsis.

• Contaminated wounds have nonreplicating organisms within their borders. These wounds will go on to heal normally.
• Colonized wounds have replicating bacteria, but these bacteria are nondestructive and contained within the wound. A hallmark of colonization is that it does not delay the wound healing process.
• Local infection or critical contamination is an intermediate level of bacterial invasion characterized by granulation tissue that has an unhealthy appearance, and wound healing that may be delayed. In this type of wound, however, tissue invasion is not present. This stage is notable for the absence of other signs of infection such as cellulitis or pus formation.
• Invasive infection occurs once bacteria have invaded through the wound bed, tissue destruction has begun, and an aggressive immune response is present. Signs and symptoms of invasive infection include pain, edema, erythema and fever. The finding of a chronic, nonhealing wound, often with pus formation and tissue necrosis is often evident.
• Sepsis occurs when the infection spread systemically, and cardiovascular instability and organ-system dysfunction develop.

The Molecular Biology of Bacterial
Infection Low levels of bacteria in wounds actually help to promote wound healing by stimulating brisk monocyte and macrophage activity. However, as their number or virulence increases, the tissue response to their presence disrupts and prolongs the inflammatory phase of wound healing, depletes the components of the complement cascade, interferes with normal clotting mechanisms, and alters leukocyte function. The level of pro-inflammatory cytokines, including interleukin-1 and tumor necrosis factor-alpha, rises and stays elevated. Elevated levels of matrix metalloproteinases and a lack of their inhibitors lead to tissue breakdown and growth factor inhibition. Bacteria also compete with local cells for oxygen, reducing its availability to these cells and stimulating an angiogenic response, leading to friable granulation tissue that is prone to bleeding.

Bacteria in Wounds
Classic teaching is that wounds with greater than 105 organisms/gram should be considered infected whereas those with a lower bacterial count should not. Although studies do show that wounds with bacterial counts higher than this heal more slowly and have a higher rate of infection, a more practical approach to diagnosing the infected wound is encouraged. As wounds mature, not only do the species of organisms present in the wound change, the wounds begin to carry a higher level of bioburden, meaning a higher baseline number of colonies without being infected. Conversely, the more virulent bacteria, such as beta-hemolytic streptococcus and some rare Clostridium species, can easily cause infection at lower quantitative levels than the more commonly occurring species. Finally, the status of the patient’s immune response has a role in the patient’s likelihood of developing an infected wound. Therefore, the surgeon is encouraged to study the appearance of the wound and the overall clinical picture when deciding whether a wound is infected. Although it is important to note the classic signs and symptoms of infection including erythema, edema, fever and an elevated white blood cell count, recent studies attempting to establish evidence-based criteria for the determination of a chronic wound infection have shown that increasing pain, friable granulation tissue, foul odor and wound breakdown are the most sensitive indicators. Bacteria in chronic wounds often establish a biofilm. This is an extracellular, polysaccharide-rich matrix in which the organisms are embedded. Within this glycocalyx is a system of channels, like a primordial circulatory system, that allows the bacteria to remain viable with less direct dependence on the host tissue. Cells in this environment become more sessile and less metabolically active. As a result, they are resistant to host immune responses and antibiotic therapy. Biofilms often coat foreign and implanted material, making infections in this setting more difficult to treat, and certain bacteria such as Pseudomonas aeruginosa have a predilection to biofilm production.

Bacteria Occurrence (%)
Staphylococcus aureus 20 Coagulase-negative staphylococci 14 Enterococci 12 Escherichia coli 8 Pseudomonas auruginosa 8 Enterobacter species 7 Proteus mirabilis 3 Klebsiella pneumonia 3 Other streptococci 3 Candida albicans 3 Group D streptococci 2

Clinical Evaluation
A thorough history includes information related to the chronicity of the wound, any changes to the wound appearance, and details that should make the clinician suspicious of a more invasive bacterial involvement (e.g., pain, fever). Mitigating factors such as comorbid conditions that could lead to immunosuppression, the use of any immunosuppressive medications, previous radiation in the wound area and the overall functional status of the patient are important to explore. In addition to a white blood cell count and blood cultures, laboratory tests can include the erythrocyte sedimentation rate and C-reactive protein. Although not specific, in a patient with no recent history of surgery or acute illness, their value is in helping to determine the level of systemic response to a wound and in helping to determine the presence of a deep wound infection. When examining a wound, its depth and width should be measured and a careful inspection and probing should be done. Attention to findings such as erythema at least 5 mm beyond the wound edges, expressed pus, necrotic debris or granulation tissue that is dark, friable or heaped above the wound edges can help to determine the extent of infection. Foreign bodies such as old strands of gauze should be removed and the presence of underlying foreign material such as sutures or mesh should be ruled out. Care must be taken to ensure that wounds overlying osseous structures do not have any exposed bone at their base that would suggest the presence of osteomyelitis. As stated earlier, bacterial cultures can help to make a diagnosis and guide appropriate therapy. In a wound that has been appropriately cleaned and prepared, a swab of the deeper tissue can give a qualitative notion of which bacteria are present. It does not, however, allow the clinician to quantitate the amount of bacteria within the wound. For this, the gold standard is a biopsy culture. A punch biopsy is taken and ground into a liquid state from which serial dilutions are cultured. A measure of colonies per milligram can then be reported.

Treatment
Antibiotics are ineffective in penetrating chronic, nonhealing wounds. Debridement is the best option for clearing bacterial loads and removing nonviable tissue. If not performed, necrotic material can release endotoxins that inhibit keratinocyte migration and matrix production, and can prolong the inflammatory response, promoting matrix-destroying proteases. Methods of debridement include sharp, mechanical, chemical and biodebridement. Sharp, or surgical debridement affords the luxury of speed, since it can be performed at the bedside with nothing more than scissors and a pair of forceps. More extensive debridement may require anesthesia, and should be performed in the operating room. Mechanical debridement is the eradication of dead tissue by the sequential changes of dressings that are inserted moist into the wound and removed after they are allowed to dry. Exudative and necrotic tissues adhere to the drying gauze and are pulled out of the wound with the gauze. This technique has only a limited ability to remove structurally intact or strongly adherent devitalized tissue. The classic “wet-to-dry” dressing is a mechanically debriding dressing. Chemical debriding agents are enzymatic compounds that break down tissue. They are most effective in moderately sized areas of necrosis or in those patients that will not tolerate an operation. In order to gain maximum benefit, larger eschars should be cross-hatched or excised to allow for better penetration of the agent. The papain-containing cream, Accuzyme®, is commonly used for this purpose. Biodebridement involves the application of sterile maggots into a wound for periods of 48-72 hours. The maggots feed on, and thus remove dead tissue before being irrigated out. This process can be repeated as necessary. Needless to say, it is not a commonly used technique. Antibiotics do have a role in the treatment of chronic, infected wounds once debridement has achieved healthy wound borders. Empiric antibiotics should be selected based on the bacteria that are likely to be involved. For example, empiric antibiotics for wounds near the oropharynx and diabetic foot wounds should include coverage for anaerobic species. The Gram stain can give a general idea of whether Gram-positive, Gram-negative or a combination of bacteria is present. Once culture results return over the subsequent 2-3 days, antibiotic coverage should be tailored to the involved organisms. Topical antibiotic preparations can help to reduce bacterial load and can be used with some success in an adjuvant setting in the select wound population. Prudence should be taken with their use, however, because many of these preparations also impair the function of the superficial cells necessary for wound healing. They should never be used in wounds related to venous disease, as these wounds are more prone to sensitivity reactions. Examples include: iodine or iodophor paint, sodium hypochlorite solution, hydrogen peroxide, acetic acid, antibiotic creams or the newer cadhexomer iodine and nanocrystalline silver. For wounds that arise in the setting of underlying pathology, treating the disease process can increase the speed and likelihood of wound healing. For venous stasis ulcers, reducing edema fluid with Unna boot compression, elevation and diuresis can improve oxygen delivery and thus cellular function. Patients with diabetic foot ulcers should have their blood sugar strictly controlled given the deleterious effects of hyperglycemia on neutrophil and monocyte function. If ischemia is believed to be contributing to the etiology or chronicity of a wound, smoking cessation and elimination of dehydration and anemia should all be considered in the treatment plan. Ultimately arterial revascularization with or without surgical reconstruction using local or microvascular flaps may be necessary.

Hidradenitis Suppurativa
This condition is due to infection of the apocrine sweat glands, most commonly in the axillary, perineal and groin regions. It results in recurrent, draining abscesses and sinus tracts that can lead to severe pain and debilitation. Lesions in the axilla that heal may scar and secondarily cause contracture limiting arm motion. Active infection should be treated with a 1-2 week course of oral antibiotics and is usually due to Gam positive cocci. Cultures should always be taken since other bacterial infections can occur, and the antibiotic should be appropriately selected. Surgical treatment consists of full-thickness excision of the infected dermis and any involved subcutaneous fat. Primary closure can be obtained in small- to moderate-sized wounds without active infection. Larger defects, or those that are grossly infected, should not be closed primarily. They should be allowed to granulate with dressing changes, followed by split-thickness skin grafting or healing by secondary intention. Incomplete excision of the involved tissue is common due to retained sinus tracts or deep infected glands. When this occurs, there is a high likelihood of recurrence and skin graft failure.

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Tissue Expansion

Introduction

Tissue expansion relies on the ability of skin and soft tissues to generate in response to tension. In plastic surgery, tension is generated by implanting a subcutaneous balloon (expander) that is inflated over a period of weeks; new tissue is generated in response to the constant stretch caused by the progressive inflation of this expander. This tissue can be used to reconstruct extirpative or traumatic defects such as those encountered after mastectomy, burn excision, or removal of giant nevi.

Biological Basis of Tissue Expansion

A number of studies support the concept that the increase in skin surface area after expansion is due to the generation of new tissue rather than the stretching of existing skin. In culture, mechanical stress induces fibroblast and epidermal hyperplasia. These cells preserve their phenotype without malignant degeneration. This observation is supported by the fact that there has never been a reported case of skin malignancy secondary to tissue expansion.

From a histological standpoint, adult and pediatric skin responds to expansion in the same manner. Within 1 week of expansion, the epidermis begins to thicken and the dermis thins. The skin appendages do not change. The subcutaneous fat and muscle atrophy. Cellular proliferation reduces the resting tension of the skin over time, enabling another round of expansion to take place. Once the process is complete, the expanded skin eventually returns to its baseline thickness. The vessels of the skin and subcutaneous tissue also resume their pre-expanded size and number; however anecdotally, some flaps demonstrate increased vascularity.

Indications

In general terms, expansion of tissue is used to improve rotation, transposition or advancement of local or regional flaps, or to increase the harvest of full-thickness skin grafts. Recently, tissue expansion has been successfully applied to myocutaneous and free flaps. In adults, aside from their use in breast reconstruction, tissue expanders are used primarily for secondary burn and trauma reconstruction in the head and neck region. In the pediatric population, expanders have been used in a multitude of reconstructive procedures. The most common indication in children is to reconstruct defects left by excision of giant congenital nevi. Tissue expansion is contraindicated in infected skin. Although expansion is possible in radiated or scarred tissue, it is associated with a much higher complication rate and should be avoided whenever possible.

Technique

Expanders come in a variety of shapes and sizes, and there is no absolute ideal expander for a given site or condition. Expanders can have either internal or external filling ports. Most experienced surgeons recommend using remote ports. These should be placed away from the expander. Internal ports have both a higher failure rate and a greater incidence of accidental expander rupture. In children, the use of internal ports is associated with a higher rate of exposure of the expander due to the pressure exerted on the skin by the port. Whenever possible, the incision should be placed within tissue destined to be excised, as in the case of congenital nevi. Straight incisions along the border of the defect should be avoided because this will enlarge the defect and may interfere with flap coverage. An alternative is to use a U- or V-shaped incision that is hidden and remote from the defect. Such incisions should be perpendicular to the direction of expansion in order to maximize skin blood supply. When doing serial expansion, longitudinal blood supply must be preserved. This holds true especially in the trunk and extremities.

The expander should be placed on top of the deep fascia (or subgaleal in the scalp), unless the plan is to incorporate muscle into the expanded flap. The pocket should always be larger than the base diameter of the expander. Blunt dissection in a single fascial plane is safest for preserving blood supply. Most surgeons overinflate tissue expanders beyond the manufacturer’s recommended maximum capacity. Studies have demonstrated that significant overinflation is possible before weakening or rupturing. The rate of inflation is variable and largely based on surgeon preference. Patient comfort and signs of tissue perfusion, such as tension, color, and capillary refill, guide the filling rate. Filling is usually initiated one week after surgery.

Tissue expansion should continue until the expanded area is larger than the defect, because of the length that is lost upon advancement and inset of the flap. The use of rotation and transposition flaps enables the transfer of tension from the tip of the flap more proximally to its base. A single or double back-cut can be performed prior to inset in order to gain extra length. Lastly, the donor site should be closed in layers after the implant capsule is excised. Pre-expansion of distant pedicle- or free-flaps facilitates closure of otherwise tight donor sites.

Intraoperative Expansion

Most surgeons fill the expanders intraoperatively with sufficient saline to eliminate dead space and tamponade raw surfaces to help prevent postoperative bleeding. There is, however, an alternative to traditional prolonged expansion. Immediate intraoperative expansion combined with broad undermining of the defect can help reduce the tension that occurs on the distal parts of a local flap. In rapid expansion, the skin initially expands due to its elasticity and the displacement of interstitial fluid. Within minutes, the alignment of the collagen fibers changes due to the stretch. This process yields up to 20% more tissue for flap coverage. Intraoperative expansion is indicated for relatively small defects, such as in coverage of defects of the ear.

Scalp

Although tissue expansion does not increase the number of hair follicles, the size of the hair-bearing region can be doubled without a noticeable decrease in hair density. As such, tissue expansion may be used a means of treating male pattern baldness in addition to reconstructing the scalp. Expanders are most commonly placed in the occipital or posterior parietal regions. They should be placed under the galea, superficial to the periosteum. It usually requires 6-8 weeks to complete the expansion in adults, and up to 12 weeks in children. Radial scoring of the galea at the time of surgery can speed the process. Once the expansion is complete, flaps are advanced or transposed, ideally based on named arteries of the scalp. It is important to orient flaps so that the correct direction of hair growth is maintained. Although galeal scoring or capuslotomy incisions can be useful, wide undermining is a safer method of recruiting tissue.

Forehead

The brow position is the most important structure to preserve during forehead expansion. When possible, two or more expanders are used with incisions hidden within the hairline. For mid-forehead lesions, bilateral, temporal expanders are used, and the skin is advanced medially based on the superficial temporal arteries. Expanders should be placed deep to the frontalis muscle. Expansion can usually begin 7-10 days postoperatively. When a large forehead flap is required for nasal reconstruction, the forehead skin can be pre-expanded prior to flap transfer.

Face and Neck

The skin of the neck and face is relatively thin. Therefore, multiple expanders with smaller volumes are preferable to a single large expander. In general, however, a single larger expander is preferable to several smaller expanders. Careful planning is essential in determining where to place the expanders, and where incisions should be located. Considerations such as preserving aesthetic units, matching skin color, avoiding distortion of the eyelids and oral commissure, and facial symmetry are all essential. The expander is usually placed above the platysma muscle in order to avoid risk of facial nerve injury and to keep the flap from being excessively bulky. The expanded flaps can be advanced, rotated, or transposed. Incisions should be placed in skin creases such as the nasolabial fold. Expanding the hairless skin adjacent to the mastoid region can increase the available tissue for reconstructive procedures of the ear. The skin above the clavicle can be expanded to provide full-thickness skin grafts to the face.

Trunk

Unlike the head and neck, there are very few critical landmarks on the trunk that must be preserved. Aside from the breast and nipple-areola complex, distortion of the skin and soft tissues of the trunk is well-tolerated. For defects requiring excision, multiple expanders surrounding the defect are often employed. Many myocutaneous flaps of the trunk, such as the latissimus dorsi, TRAM and pectoralis flaps, can be pre-expanded in order to increase their size and facilitate donor site closure. Expanders can also be used to expand the skin of the abdomen for use as a donor site of full-thickness skin grafts.

Extremities

Tissue expansion in the extremities has been reported to have a higher complication rate in comparison to other regions and therefore should not be a first choice among the reconstructive options. The blood supply and drainage of the extremities is inferior to that of the trunk and head. This predisposes limbs, especially below the knee, to an increased rate of infection and wound complications. Multiple expanders are usually required in the extremites.

Complications

Proper placement and filling of tissue expanders has a steep learning curve. With experience, the complication rate drops dramatically. Among all patients, the major complication rate is about 10% and includes implant exposure, deflation, and wound dehiscence. Minor complications also occur in about 10% of patients. These include filling port problems, seroma, hematoma, infection and delayed healing.

Patients under the age of 7 have the highest risk of complications. One explanation for this is that young children are more prone to expander rupture due to external pressure on the expanded skin. Expansion in the extremities caries twice the risk of complication compared to other regions. The use of tissue expansion in burn reconstruction and soft tissue loss has a 15-20% major complication rate, whereas for congenital nevi it is 5-7%. Finally, tissue that has undergone serial expansion (two or more prior expansions) is at a higher risk for a major complication.

Pearls and Pitfalls

Tissue expansion should be avoided in infected fields, in close proximity to a malignancy, in skin-grafted regions, and in skin that has been previously radiated.

Every effort should be made to place the incision as far as possible from the region to be expanded, unless the incision can be incorporated into the tissue that is destined to be excised. If the incision is subject to the tension of expansion, it becomes at risk for dehiscence and hypertrophic scarring.

A key point in tissue expansion is the development of an adequately sized pocket. If the pocket is too small, expansion will likely fail. If the pocket is overly large, the expander can shift positions, resulting in expansion of the wrong tissue. Textured expanders are less likely to shift after placement.

The rate of expansion is variable and depends both on the body site as well as patient factors. Some skin is more amenable to expansion, and some patients can tolerate the discomfort better than others. It is possible to be overly aggressive with the rate of expansion, resulting in overlying skin ischemia, necrosis and ultimately implant extrusion.

As a general rule, the diameter of the expanded flap should be 2-3 times the diameter of the skin that is to be excised

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